Adrenergic nerves mediate the venoconstrictor response to PVN stimulation.

Veins play an important role in the control of venous return, cardiac output and cardiovascular homeostasis. However, the central nervous system sites and effector systems involved in modulating venous function remain to be fully elucidated. The hypothalamic paraventricular nucleus (PVN) is an important site modulating autonomic outflow to the cardiovascular system. Venous tone can be modulated by sympathetic nerves or by adrenal catecholamines. The present study assessed the relative contribution of these autonomic effector systems to the venoconstrictor response elicited by stimulation of the hypothalamic paraventricular nucleus. Male Sprague-Dawley rats were subjected to sham operation or bilateral adrenal demedullation fitted with PVN guide cannulae and fitted with catheters for recording arterial pressure (AP) and intrathoracic vena caval pressure (VP). A latex balloon was advanced into the right atrium. MCFP was calculated from the AP and VP recorded after 4 s of right atrial occlusion. MCFP = VP + (AP - VP)/60. Mean arterial pressure (MAP), heart rate (HR), VP and MCFP responses to injections of BMI (25 ng/side) into the PVN were recorded from conscious rats to avoid the complicating effects of anesthesia. In sham-operated rats, injection of BMI into the PVN increased MAP by 13 +/- 3 mm Hg and HR by 56 +/- 6 bpm. MCFP was also increased significantly by 0.98 +/- 0.15 mm Hg indicating an increase in venomotor tone. Adrenal medullectomy did not affect the pressor (DeltaMAP = 12 +/- 2 mm Hg), tachycardic (DeltaHR = 48 +/- 7 bpm) or venoconstrictor (DeltaMCFP = 0.73 +/- 0.11 mm Hg) responses. Ganglionic blockade abolished the PVN-induced responses in both groups of rats. In a separate group, pretreatment with the adrenergic neuron blocker, guanethidine (20 mg/kg), also abolished the PVN-mediated venoconstrictor responses. Conversely, selective beta2 adrenergic receptor blockade did not affect MCFP responses to BMI. These data indicate that adrenomedullary catecholamines are not necessary for full expression of the venoconstrictor response to PVN stimulation.

Naloxone microinjected into the arcuate nucleus has differential effects on ventilation in male and female rats.

The arcuate nucleus of the hypothalamus, a highly sexually dimorphic brain region, has been called the bed nucleus for endogenous opioids. The potential contribution of opioids in this nucleus to modulate control of ventilation in male and female rats has not been investigated. The purpose of the present study is to determine the effect of microinjecting naloxone, an opioid receptor antagonist, into the arcuate nucleus of awake male and female rats on ventilation, oxygen consumption, heart rate, and blood pressure. Results of this study demonstrate that naloxone at doses of 1.5 and 3.0 nmol relative to vehicle caused a depression of ventilation due to a decrease of both frequency of breathing and tidal volume in male rats and a decreased response to a hypercapnic challenge in female rats. Although there were gender differences noted in oxygen consumption, heart rate, blood pressure, and ventilatory response to a hypoxic challenge, only oxygen consumption was significantly affected by naloxone. Potential mechanisms whereby naloxone may act to depressing ventilation are discussed.

Disinhibition of the hypothalamic paraventricular nucleus increases mean circulatory filling pressure in conscious rats.

Venous capacitance plays an important role in the control of cardiac output. However, the central nervous system sites and neurochemical signals involved in modulating venous function remain to be fully elucidated. The hypothalamic paraventricular nucleus (PVN) is an important site modulating autonomic outflow to the cardiovascular system. The present study tested the hypothesis that removal of tonic GABAergic tone in the PVN would increase peripheral venous tone. Mean circulatory filling pressure was used as an index of venous tone. Arterial pressure, venous pressure, heart rate, and mean circulatory filling pressure (MCFP) were monitored in conscious male Sprague Dawley rats. The rats were challenged with microinjections of bicuculline methiodide (BMI) (25 ng) or vehicle (artificial cerebrospinal fluid) into the PVN. In one group of rats, BMI injections were performed before and after ganglionic blockade with chlorisondamine hydrochloride (10 mg/kg) and atropine (0.4 mg/kg) given subcutaneously. In a second group, BMI injections were performed in chlorisondamine-treated rats whose blood pressure had been returned to control with an infusion of norepinephrine. Injection of bicuculline into the PVN increased MAP (14 +/- 2 to 18 +/- 2 mmHg) and HR (49 +/- 12 to 74 +/- 14 bpm). MCFP also increased significantly by 1.00 +/- 0.17 to 1.39 +/- 0.18 mmHg, indicating an increase in the driving pressure for venous return. Injection of the vehicle did not affect these variables. In both groups, ganglionic blockade significantly attenuated the bicuculline-induced increases in MAP, HR and MCFP. These data indicate that sympathetic drive from the PVN to the venous system is under tonic GABAergic control.

Acute stress increases venomotor tone in conscious rats.

This study tested the hypothesis that acute psychological stress causes venoconstriction. Male Sprague-Dawley rats were instrumented with indwelling catheters in a femoral artery and vein and a balloon-tipped catheter in the right atrium. Mean arterial pressure (MAP), venous pressure, heart rate (HR), and mean circulatory filling pressure (MCFP) were monitored in conscious rats. Air-jet stress was performed before and after treatment with saline, chlorisondamine, phentolamine, or prazosin. Air-jet stress caused MAP, HR, and MCFP to increase by 10 +/- 1 mmHg, 31 +/- 4 beats/min, and 0.95 +/- 0.09 mmHg, respectively. Treatment with either chlorisondamine or phentolamine was equally effective in abolishing the stress-induced increases in MAP, HR, and MCFP. Prazosin treatment abolished the pressor response to air-jet stress but did not significantly affect the HR and MCFP responses. In contrast, pretreatment with the alpha 2-receptor antagonist rauwolscine hydrochloride abolished both the MAP and MCFP responses to air-jet stress but did not affect the HR response. These findings indicate that venoconstriction is an important component of the cardiovascular response to acute psychological stress. Stress-induced venoconstriction appears to be mediated primarily via the alpha 2-receptor subtype.